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hepatitis

 
American Heritage Dictionary:

hep·a·ti·tis

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(hĕp'ə-tī'tĭs) pronunciation
n., pl., -tit·i·des (-tĭt'ĭ-dēz').
Inflammation of the liver, caused by infectious or toxic agents and characterized by jaundice, fever, liver enlargement, and abdominal pain.


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Britannica Concise Encyclopedia:

hepatitis

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Inflammation of the liver. There are seven known types of viral hepatitis (A-G). Types A, spread mainly through food contaminated with feces, and B, transmitted sexually or by injection, cause jaundice and flulike symptoms. The hepatitis C virus spreads mostly by shared needles in intravenous drug use and can cause liver cirrhosis and cancer after a long latent period. Until recently there was no test to detect it in blood, and many people were exposed through blood transfusions. Hepatitis D becomes active only in the presence of type B; it causes severe chronic liver disease. Type E, like Type A, is transmitted by contaminated food or water; its symptoms are more severe than Type A's and can result in death. The hepatitis F virus (HFV), which was first reported in 1994, is spread like Type A and E. The hepatitis G virus (HGV), isolated in 1996, is believed to be responsible for many sexually transmitted and bloodborne cases of hepatitis. Vaccines exist for types A and B (the second also prevents type D). Drug treatment for B and C is not always effective. The other types may not need drug treatment. Chronic active hepatitis causes spidery and striated skin markings, acne, and abnormal hair growth. It results in liver tissue death (necrosis) progressing to cirrhosis. Alcoholic hepatitis, from long-term overconsumption of alcohol, can be reversed and cirrhosis prevented by early treatment including quitting or sharply reducing drinking. Other drugs can also cause noninfectious hepatitis. An autoimmune hepatitis affects mainly young women and is treated with corticosteroids to relieve symptoms.

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McGraw-Hill Science & Technology Encyclopedia:

Hepatitis

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An inflammation of the liver caused by a number of etiologic agents, including viruses, bacteria, fungi, parasites, drugs, and chemicals. The most common infectious hepatitis is of viral etiology. All types of hepatitis are characterized by distortion of the normal hepatic lobular architecture due to varying degrees of necrosis of individual liver cells or groups of liver cells, acute and chronic inflammation, and Kupffer cell enlargement and proliferation. There is usually some degree of disruption of normal bile flow, which causes jaundice. The severity of the disease is highly variable and often unpredictable. See also Liver.

A frequently occurring form of hepatitis is caused by excessive ethyl alcohol intake and is referred to as alcoholic hepatitis. It usually occurs in chronic alcoholics and is characterized by fever, high white blood cell count, and jaundice. Some drugs are capable of damaging the liver and can occasionally cause enough damage to produce clinical signs and symptoms. Among these drugs are tetracycline, methotrexate, anabolic and contraceptive steroids, phenacetin, halothane, chlorpromazine, and phenylbutazone.

Clinical features of hepatitis include malaise, fever, jaundice, and serum chemical tests revealing evidence of abnormal liver function. In most mild cases of hepatitis, treatment consists of bedrest and analgesic drugs. In those individuals who develop a great deal of liver cell necrosis and subsequently progress into a condition known as hepatic encephalopathy, exchange blood transfusions are often used. This is done with the hope of removing or diluting the toxic chemicals thought to be the cause of this condition. Chronic hepatitis is a condition defined clinically by evidence of liver disease for at least 6 consecutive months. See also Alcoholism; Liver disorders.

Hepatitis C is a disease of the liver caused by the hepatitis C virus (HCV). The prevalence of HCV infection worldwide is 3% (170 million people), with infection rates in North America ranging from 1 to 2% of the population. A simulation analysis estimated that in the period from 1998 to 2008 there will be an increase of 92% in the incidence of cirrhosis of the liver, resulting in a 126% increase in the incidence of liver, failures and a 102% increase in the incidence of hepatocellular carcinoma (HCC), all attributed to HCV.

Hepatitis C virus can be transmitted only by blood-to-blood contact. With the institution of screening of blood, intravenous drug use has become the major source of transmission in North America. Approximately 89% of people who use intravenous drugs for one year become infected with HCV.

Management strategies can be divided into three main areas: surveillance of patients with chronic HCV infection who have not developed cirrhosis; surveillance of patients with established cirrhosis; and strategies to eradicate HCV.

Oxford Food & Nutrition Dictionary:

hepatitis

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Inflammatory liver disease, characterized by jaundice, abdominal pain, and anorexia. May be due to bacterial or viral infection, alcohol abuse, or various toxins. Treatment is usually conservative, with a very low fat diet (secretion of bile is impaired) and complete abstinence from alcohol.

Even after recovery, people may continue to be carriers of the virus, especially for hepatitis B and C, which are transmitted through blood and other body fluids. Liver cancer and cirrhosis are more common among people who have suffered from hepatitis B or C.

Oxford Dictionary of Sports Science & Medicine:

hepatitis

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Inflammation of the liver, commonly caused by viruses, but also by alcohol, drugs, and overexposure to toxic chemicals. There are at least three different forms of hepatitis: hepatitis A (infectious hepatitis) is spread via viruses taken in with food and excreted in the faeces; hepatitis B (serum hepatitis) is transmitted sexually, or via infected blood or blood products; and hepatitis C, which is transmitted primarily by blood and blood products. Hepatitis B has been recorded in orienteers who run in woods and brush past undergrowth carrying the virus from an infected person who has been scratched. Rules specifying clothing to be worn in orienteering and other outside sports are aimed at minimizing the risk of these and other diseases (see also Lyme disease). Carriers of the hepatitis B virus are not excluded from sport, but it is important that any injury that causes bleeding is cleaned and secured immediately. Although hepatitis B is a relatively rare infection among athletes, it has a relatively high theoretical risk of transmission; therefore, sensible precautions should be taken and good hygiene practiced.

Columbia Encyclopedia:

hepatitis

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hepatitis (hĕp'ətī'tĭs), inflammation of the liver. There are many types of hepatitis. Causes include viruses, toxic chemicals, alcohol consumption, parasites and bacteria, and certain drugs. Symptoms of hepatitis are nausea, fever, weakness, loss of appetite, sudden distaste for tobacco smoking, and jaundice.

A number of viruses can cause acute viral hepatitis. Five have been identified and named hepatitis A through E. At least 10 other viruses are under study. Hepatitis A, also called infectious hepatitis, occurs sporadically or in epidemics, the virus being present in feces and transmittable via contaminated food (e.g., food prepared by an infected person with unwashed hands or fresh food washed or grown with contaminated water) or water. A person with active infection can spread it by physical contact. The disease usually resolves on its own. Exposed persons can be protected by injections of gamma globulin. A vaccine was made available in 1995 and is recommended for children at risk for the virus.

Hepatitis B, also called serum hepatitis, was commonly transmitted through blood transfusions until the 1970s, when screening tests were introduced. Intravenous-drug abusers remain a high-risk group because of the sharing of needles. It is also spread by sexual transmission and from mother to baby at birth. Some infected individuals, particularly children, become chronic carriers of the virus. Hepatitis B can progress to chronic liver disease and is associated with an increased risk of developing liver cancer. A vaccine, available since 1981, is recommended for all infants and others at risk for the virus. Alpha-interferon was approved as a treatment in 1992.

Hepatitis C, formerly called non-A, non-B hepatitis, is also transmitted by contaminated blood transfusions and by sharing of needles among drug abusers, although in many cases no source can be identified. It is the most common form of chronic liver disease in the United States. Many of those infected have no symptoms but become carriers, and the virus may eventually cause liver damage. Blood banks routinely screen for hepatitis C. Alpha-interferon is used also to treat hepatitis C, in combination with the drug ribavirin, and may result in a long-term cure.

Hepatitis D, or delta hepatitis, affects only people with hepatitis B; those infected with both viruses tend to have more severe symptoms. Hepatitis E is spread by consuming feces-contaminated food or water. It is common in Mexico, Africa, and Asia and is especially serious in pregnant women.

Hepatitis can be incurred as a complication of several other disorders in addition to viral infection, among them amebic dysentery, cirrhosis of the liver, and mononucleosis. Also, alcohol, carbon tetrachloride, some tranquilizers and antibiotics, and many other substances can produce a toxic reaction in the liver, resulting in toxic hepatitis.

Dictionary of Cultural Literacy: Health:

hepatitis

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(hep-uh-teye-tis)

An inflammation of the liver. Hepatitis is most often caused by a virus, but it can be the result of exposure to certain toxic agents, such as drugs or chemicals. One viral form of the disease is spread by contaminated food and water, and other forms by contaminated injection needles and blood transfusions. Symptoms of hepatitis include fever and jaundice.

Oxford Dictionary of Biochemistry:

hepatitis

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any inflammatory disease of the liver. In humans the most common cause is infection with a virus or an amoeba. Hepatitis A is caused by a single-stranded RNA picornavirus, for which there is a killed virus vaccine, virus having been grown in tissue culture. Hepatitis B is caused by a double-stranded DNA virus of the Hepadnaviridae family forming a spherical virion often referred to as the Dane particle. It is especially virulent and is associated with the development of primary liver tumours — the incidence of these is particularly high in China. The antigens may be in the form of spherical particles designated HBsAg; principal components include gp27, which is a glycosylated form of p24, and a 42 kDa protein. HBsAg is produced in recombinant yeast, the particles being similar to those found in the plasma of infected individuals and providing a very effective vaccine. Hepatitis C, formerly called 'non-A non-B', is caused by a single-stranded RNA virus, for which there is no vaccine. Hepatitis D virus is a satellite virus of hepatitis B virus and contains a circular single — stranded RNA genome (≈1700 nt). Its replication requires the antigen HDAg — the only protein encoded by the virus — and RNA polymerase II. HDAg-S (195 amino acids) activates replication of the virus. HDAg-L is the former with a 19-residue C-terminal extension; it inhibits replication and directs assembly of the virion. HDAg-S shares 21% sequence identity with NELF-A. Other forms are hepatitis E, F, and G.

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Saunders Veterinary Dictionary:

hepatitis

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Inflammation of the liver which may be toxic or infectious in origin; characterized by signs due to diffuse injury to the liver. See also liver dysfunction. There are a number of etiologically specific hepatitides which are listed under their individual headings. They are avian vibrionic hepatitis, infectious canine hepatitis (see below), infectious necrotic hepatitis, duck hepatitis, turkey hepatitis, inclusion body hepatitis, mouse hepatitis, postvaccinal hepatitis, toxemic jaundice, and those caused by fasciola and fascioloides, cysticercus, and plant toxins including pyrrolizidine alkaloids, sporidesmin, aflatoxin. See also hepatosis dietetica.

  • h. A, B, C, D and E viruses — causes of hepatitis in humans and some nonhuman primates.
  • avian vibrionic h. — a disease of domesticated poultry which has disappeared from those areas in the USA which were its sole habitat. Vibrio-like organisms were isolated from the outbreaks which occurred.
  • cholangiolitic h. — see cholangiohepatitis.
  • chronic active h. — a chronic inflammatory liver disease in humans, probably of several types with different causes, but with distinctive histopathological features of piecemeal necrosis, bridging fibrosis and active cirrhosis. A similar, but not identical disease of unknown etiology has been described in dogs.
  • copper-induced h. — see bedlington terrier copper-associated hepatopathy.
  • duck h. — see duck hepatitis.
  • gosling h. — see goose hepatitis.
  • infectious canine h. — an acute, highly contagious disease, occurring mainly in young dogs, caused by canine adenovirus type 1. Many dogs experience subclinical infections. Those with clinical signs show fever, depression, vomiting and abdominal pain. The course is short and in severe cases death occurs within a few days. Peracute infections occur in very young puppies. Mild infections may cause only vague signs of malaise and anorexia and many cases are not diagnosed. Dogs recovering from infection sometimes develop corneal edema (‘blue eye’). A chronic hepatitis is reported as an occasional sequela. The disease can be prevented by vaccination.
  • mouse h. — a coronavirus disease which causes heavy losses in baby mice. It is characterized by tremor, jaundice and hemoglobinuria.
  • mycotic h. — commonly caused in cattle by extension from mycotic rumenitis due to lactic acid indigestion and damage to ruminal epithelium.
  • necrotic h. — see infectious necrotic hepatitis.
  • porcine h. E virus — an enteric virus of pigs related to human hepatitis E that is not known to be pathogenic.
  • toxipathic h. — hepatitis caused by toxins, especially ingested plant toxins, e.g. some pyrrolizidine alkaloids, sporidesmin, aflatoxin.
  • trophopathic h. — see trophopathic hepatitis.
  • turkey h. — see turkey hepatitis.
  • h. X — a hepatoxic disease of dogs and pigs caused by aflatoxins. See also mycotoxicosis.
Mosby's Dental Dictionary:

hepatitis

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(hep′ə-tī′tis)
n

An inflammation of the liver.

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categories related to 'hepatitis'

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For a list of words related to hepatitis, see:
  • Diseases and Infestations - hepatitis: inflammation of liver, due to virus transmitted by food or drink (infectious hepatitis) or blood on needle or in transfusion (serum hepatitis), causing fever and jaundice

Bradford's Crossword Solver's Dictionary:

hepatitis

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Wikipedia on Answers.com:

Hepatitis

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Hepatitis
Classification and external resources

Alcoholic hepatitis evident by fatty change, cell necrosis, Mallory bodies
ICD-10 K75.9
ICD-9 573.3
DiseasesDB 20061
MeSH D006505

Hepatitis (plural hepatitides) is a medical condition defined by the inflammation of the liver and characterized by the presence of inflammatory cells in the tissue of the organ. The name is from the Greek hepar (ἧπαρ), the root being hepat- (ἡπατ-), meaning liver, and suffix -itis, meaning "inflammation" (c. 1727).[1] The condition can be self-limiting (healing on its own) or can progress to fibrosis (scarring) and cirrhosis.

Hepatitis may occur with limited or no symptoms, but often leads to jaundice, anorexia (poor appetite) and malaise. Hepatitis is acute when it lasts less than six months and chronic when it persists longer. A group of viruses known as the hepatitis viruses cause most cases of hepatitis worldwide, but it can also be due to toxins (notably alcohol, certain medications, some industrial organic solvents and plants), other infections and autoimmune diseases.

Contents

Signs and symptoms

Acute

Initial features are of nonspecific flu-like symptoms, common to almost all acute viral infections and may include malaise, muscle and joint aches, fever, nausea or vomiting, diarrhea, and headache. More specific symptoms, which can be present in acute hepatitis from any cause, are: profound loss of appetite, aversion to smoking among smokers, dark urine, yellowing of the eyes and skin (i.e., jaundice) and abdominal discomfort. Physical findings are usually minimal, apart from jaundice in a third and tender hepatomegaly (swelling of the liver) in about 10%. Some exhibit lymphadenopathy (enlarged lymph nodes, in 5%) or splenomegaly (enlargement of the spleen, in 5%).[2]

Acute viral hepatitis is more likely to be asymptomatic in younger people. Symptomatic individuals may present after convalescent stage of 7 to 10 days, with the total illness lasting 2 to 6 weeks.[3]

A small proportion of people with acute hepatitis progress to acute liver failure, in which the liver is unable to clear harmful substances from the circulation (leading to confusion and coma due to hepatic encephalopathy) and produce blood proteins (leading to peripheral edema and bleeding). This may become life-threatening and occasionally requires a liver transplant.

Chronic

Chronic hepatitis often leads to nonspecific symptoms such as malaise, tiredness and weakness, and often leads to no symptoms at all. It is commonly identified on blood tests performed either for screening or to evaluate nonspecific symptoms. The occurrence of jaundice indicates advanced liver damage. On physical examination there may be enlargement of the liver.[4]

Extensive damage and scarring of liver (i.e. cirrhosis) leads to weight loss, easy bruising and bleeding tendencies, peripheral edema (swelling of the legs) and accumulation of ascites (fluid in the abdominal cavity). Eventually, cirrhosis may lead to various complications: esophageal varices (enlarged veins in the wall of the esophagus that can cause life-threatening bleeding) hepatic encephalopathy (confusion and coma) and hepatorenal syndrome (kidney dysfunction).

Acne, abnormal menstruation, lung scarring, inflammation of the thyroid gland and kidneys may be present in women with autoimmune hepatitis.[4]

Pathology

The liver, like all organs, responds to injury in a limited number of ways and a number of patterns have been identified. Liver biopsies are rarely performed for acute hepatitis and because of this the histology of chronic hepatitis is better known than that of acute hepatitis.

Acute

In acute hepatitis the lesions (areas of abnormal tissue) predominantly contain diffuse sinusoidal and portal mononuclear infiltrates (lymphocytes, plasma cells, Kupffer cells) and swollen hepatocytes. Acidophilic cells (Councilman bodies) are common. Hepatocyte regeneration and cholestasis (canalicular bile plugs) typically are present. Bridging hepatic necrosis (areas of necrosis connecting two or more portal tracts) may also occur. There may be some lobular disarray. Although aggregates of lymphocytes in portal zones may occur these are usually neither common nor prominent. The normal architecture is preserved. There is no evidence of fibrosis or cirrhosis (fibrosis plus regenerative nodules). In severe cases prominent hepatocellular necrosis around the central vein (zone 3) may be seen.

In submassive necrosis – a rare presentation of acute hepatitis – there is widespread hepatocellular necrosis beginning in the centrizonal distribution and progressing towards portal tracts. The degree of parenchymal inflammation is variable and is proportional to duration of disease.[5][6] Two distinct patterns of necrosis have been recognised: (1) zonal coagulative necrosis or (2) panlobular (nonzonal) necrosis.[7] Numerous macrophages and lymphocytes are present. Necrosis and inflammation of the biliary tree occurs.[8] Hyperplasia of the surviving biliary tract cells may be present. Stromal haemorrhage is common.

The histology may show some correlation with the cause:

  • Zone 1 (periportal) occurs in phosphorus poisoning or eclampsia.
  • Zone 2 (midzonal) – rare – is seen in yellow fever.
  • Zone 3 (centrilobular) occurs with ischemic injury, toxic effects, carbon tetrachloride exposure or chloroform ingestion. Drugs such as acetaminophen may be metabolized in zone 1 to toxic compounds that cause necrosis in zone 3.

Where patients have recovered from this condition, biopsies commonly show multiacinar regenerative nodules (previously known as adenomatous hyperplasia).[9]

Massive hepatic necrosis is also known and is usually rapidly fatal. The pathology resembles that of submassive necrosis but is more markered in both degree and extent.

Chronic

Chronic hepatitis has been better studied and several conditions have been described.

Chronic active hepatitis was the term used to described cases of hepatitis for more than 6 months with portal based inflammation, fibrosis, disruption of the terminal plate and piecemeal necrosis. This term has now been replaced by the diagnosis of 'chronic hepatitis with piecemeal (periportal) necrosis (or interface hepatitis) with or without fibrosis.'[10]

Chronic persistent hepatitis was the term used to describe chronic hepatitis with no significant periportal necrosis or regeneration with a fairly dense mononuclear portal infiltrate. Councilman bodies are frequently seen within the lobule. This condition is now referred to as 'chronic hepatitis without piecemeal necrosis (or interface hepatitis).'[10]

Chronic lobular hepatitis was the term used to describe chronic hepatitis with persistent parenchymal focal hepatocyte necrosis (apoptosis) with mononuclear sinusoidal infiltrates. This is now referred to as 'chronic hepatitis without piecemeal necrosis (or interface hepatitis).'[10]

These terms have since been deprecated.[10] This was done because it was realised that these conditions could alter over time and what might have been regarded as a relatively benign lesion could still progress to cirrhosis. The simpler term 'chronic hepatitis' is now preferred in association with the causative agent (when known) and a grade based on the degree of inflammation, piecemeal or bridging necrosis (interface hepatitis) and the stage of fibrosis. Several grading systems have been proposed but none have been adopted universally.

Cirrhosis is a diffuse process characterized by regenerative nodules that are separated from one another by bands of fibrosis. It is the end stage for many chronic liver diseases. The pathophysiological process that results in cirrhosis is as follows: hepatocytes are lost through a gradual process of hepatocellular injury and inflammation. This injury stimulates a regenerative response in the remaining hepatocytes. The fibrotic scars limit the extent to which the normal architecture can be reestablished as the scars isolate groups of hepatocytes. This results in nodules formation. Angiogenisis (new vessel formation) accompanies scar production which results in the formation of abnormal channels between the central hepatic veins and the portal vessels. This in turn causes shunting of blood around the regenerating parenchyma. Normal vascular structures including the sinusoidal channels may be obliterated by fibrotic tissue leading to portal hypertension. The overall reduction in hepatocyte mass, in conjunction with the portal blood shunting, prevents the liver from accomplishing its usual functions – the filtering of blood from the gastrointestinal tract and serum protein production. These changes give rise to the clinical manifestations of cirrhosis.

Specific cases

Most of the causes of hepatitis cannot be distinguished on the basis of the pathology but some do have particular features that are suggestive of a particular diagnosis.

The presence of micronodular cirrhosis, Mallory bodies and fatty change within a single biopsy are highly suggestive of alcoholic injury.[11] Perivenular, pericellular fibrosis (known as 'chicken wire fibrosis' because of its appearance on trichrome or van Gieson stains) with partial or complete obliteration of the central vein is also very suggestive of alcohol abuse.

Cardiac, ischemic and venous outflow obstruction all cause similar patterns.[12] The sinusoids are often dilated and filled with erythrocytes. The liver cell plates may be compressed. Coagulative necrosis of the hepatocytes can occur around the central vein. Hemosiderin and lipochrome laden macrophages and inflammatory cells may be found. At the edge of the fibrotic zone cholestasis may be present. The portal tracts are rarely significantly involved until late in the course.

Biliary tract disease including primary biliary cirrhosis, sclerosing cholangitis, inflammatory changes associated with idiopathic inflammatory bowel disease and duct obstruction have similar histology in their early stages. Although these diseases tend to primarily involve the biliary tract they may also be associated with chronic inflammation within the liver and difficult to distinguish on histological grounds alone. The fibrotic changes associated with these disease principally involve the portal tracts with cholangiole proliferation, portal tract inflammation with neutrophils surrounding the cholangioles, disruption of the terminal plate by mononuclear inflammatory cells and occasional hepatocyte necrosis. The central veins are either not involved in the fibrotic process or become involved only late in the course of the disease. Consequently the central–portal relationships are minimally distorted. Where cirrhosis is present it tends to be in the form of a portal–portal bridging fibrosis.

Hepatitis E causes different histological patterns that depend on the host's background.[13] In immunocompetent patients the typical pattern is of severe intralobular necrosis and acute cholangitis in the portal tract with numerous neutrophils. This normally resolves without sequelae. Disease is more severe in those with preexisting liver disease such as cirrhosis. In the immunocompromised patients chronic infection may result with rapid progression to cirrhosis. The histology is similar to that found in hepatitis C virus with dense lymphocytic portal infiltrate, constant peacemeal necrosis and fibrosis.

Causes

Acute

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Chronic

Discussion

Alcoholic hepatitis

Main article: Alcoholic hepatitis

Ethanol, mostly in alcoholic beverages, is a significant cause of hepatitis. Usually alcoholic hepatitis comes after a period of increased alcohol consumption. Alcoholic hepatitis is characterized by a variable constellation of symptoms, which may include feeling unwell, enlargement of the liver, development of fluid in the abdomen ascites, and modest elevation of liver blood tests. Alcoholic hepatitis can vary from mild with only liver test elevation to severe liver inflammation with development of jaundice, prolonged prothrombin time, and liver failure. Severe cases are characterized by either obtundation (dulled consciousness) or the combination of elevated bilirubin levels and prolonged prothrombin time; the mortality rate in both categories is 50% within 30 days of onset.

Alcoholic hepatitis is distinct from cirrhosis caused by long term alcohol consumption. Alcoholic hepatitis can occur in patients with chronic alcoholic liver disease and alcoholic cirrhosis. Alcoholic hepatitis by itself does not lead to cirrhosis, but cirrhosis is more common in patients with long term alcohol consumption. Patients who drink alcohol to excess are also more often than others found to have hepatitis C.[citation needed] The combination of hepatitis C and alcohol consumption accelerates the development of cirrhosis.

Drug-induced

Main article: Hepatotoxicity

A large number of drugs can cause hepatitis:[79]

The clinical course of drug-induced hepatitis is quite variable, depending on the drug and the patient's tendency to react to the drug. For example, halothane hepatitis can range from mild to fatal as can INH-induced hepatitis. Hormonal contraception can cause structural changes in the liver. Amiodarone hepatitis can be untreatable since the long half life of the drug (up to 60 days) means that there is no effective way to stop exposure to the drug. Statins can cause elevations of liver function blood tests normally without indicating an underlying hepatitis. Lastly, human variability is such that any drug can be a cause of hepatitis.

Other toxins

Other Toxins can cause hepatitis:

Metabolic disorders

Some metabolic disorders cause different forms of hepatitis. Hemochromatosis (due to iron accumulation) and Wilson's disease (copper accumulation) can cause liver inflammation and necrosis.

Non-alcoholic steatohepatitis (NASH) is effectively a consequence of metabolic syndrome.

Obstructive

"Obstructive jaundice" is the term used to describe jaundice due to obstruction of the bile duct (by gallstones or external obstruction by cancer). If longstanding, it leads to destruction and inflammation of liver tissue.

Autoimmune

Anomalous presentation of human leukocyte antigen (HLA) class II on the surface of hepatocytes, possibly due to genetic predisposition or acute liver infection; causes a cell-mediated immune response against the body's own liver, resulting in autoimmune hepatitis.

Alpha 1-antitrypsin deficiency

In severe cases of alpha 1-antitrypsin deficiency (A1AD), the accumulated protein in the endoplasmic reticulum causes liver cell damage and inflammation.

Non-alcoholic fatty liver disease

Non-alcoholic fatty liver disease (NAFLD) is the occurrence of fatty liver in people who have no history of alcohol use. It is most commonly associated with obesity (80% of all obese people have fatty liver). It is more common in women. Severe NAFLD leads to inflammation, a state referred to as non-alcoholic steatohepatitis (NASH), which on biopsy of the liver resembles alcoholic hepatitis (with fat droplets and inflammatory cells, but usually no Mallory bodies).

The diagnosis depends on medical history, physical exam, blood tests, radiological imaging and sometimes a liver biopsy. The initial evaluation to identify the presence of fatty infiltration of the liver is medical imaging, including such ultrasound, computed tomography (CT), or magnetic resonance (MRI). However, imaging cannot readily identify inflammation in the liver. Therefore, the differentiation between steatosis and NASH often requires a liver biopsy. It can also be difficult to distinguish NASH from alcoholic hepatitis when the patient has a history of alcohol consumption. Sometimes in such cases a trial of abstinence from alcohol along with follow-up blood tests and a repeated liver biopsy are required.

NASH is becoming recognized as the most important cause of liver disease second only to hepatitis C in numbers of patients going on to cirrhosis.[citation needed]

Ischemic hepatitis

Main article: Ischemic hepatitis

Ischemic hepatitis is caused by decreased circulation to the liver cells. Usually this is due to decreased blood pressure (or shock), leading to the equivalent term "shock liver". Patients with ischemic hepatitis are usually very ill due to the underlying cause of shock. Rarely, ischemic hepatitis can be caused by local problems with the blood vessels that supply oxygen to the liver (such as thrombosis, or clotting of the hepatic artery[disambiguation needed ] which partially supplies blood to liver cells). Blood testing of a person with ischemic hepatitis will show very high levels of transaminase enzymes (AST and ALT), which may exceed 1000 U/L. The elevation in these blood tests is usually transient (lasting 7 to 10 days). It is rare that liver function will be affected by ischemic hepatitis.

Giant cell hepatitis

Giant cell hepatitis is a rare form of hepatitis (~100 cases reported) that predominantly occurs in children. Diagnosis is made on the basis of the presence of hepatocellular multinucleate giant cells.[83][84][7] Cases presenting in adults are rare and tend to be rapidly progressive.[85][86][87][88][89] The cause is currently unknown but an infectious cause is suspected.[90][91]The condition tends to improve with the use of ribivirin suggesting a viral origin.[92][93] Hepatitis E[94], hepatitis C,[95] paramyxovirus[96][97][98][99], papillomavirus[100][101] and Human herpes virus 6[102][103] have been suggested as causes. A similar condition has been reported in cats but it is not known if there is any connection between these conditions.[104]

See also

References

  1. ^ Online Etymology Dictionary
  2. ^ Ryder S, Beckingham I (2001). "Acute hepatitis". BMJ 322 (7279): 151–153. doi:10.1136/bmj.322.7279.151. PMC 1119417. PMID 11159575. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1119417. 
  3. ^ a b Bain VG, Ma M. "Ch. 14: Acute Viral Hepatitis". First principle of gastroenterology. http://www.gastroresource.com/GITextbook/en/Chapter14/14-4.htm.  (an online text book)
  4. ^ a b Chronic hepatitis at Merck Manual of Diagnosis and Therapy Home Edition
  5. ^ Boyer JL, Klatskin G (1970). "Pattern of necrosis in acute viral hepatitis. Prognostic value of bridging (subacute hepatic necrosis)". N. Engl. J. Med. 283 (20): 1063–71. doi:10.1056/NEJM197011122832001. PMID 4319402. 
  6. ^ Gimson AE (July 1996). "Fulminant and late onset hepatic failure". Br J Anaesth 77 (1): 90–8. PMID 8703634. http://bja.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=8703634. 
  7. ^ a b Kirsch R, Yap J, Roberts EA, Cutz E (April 2009). "Clinicopathologic spectrum of massive and submassive hepatic necrosis in infants and children". Hum. Pathol. 40 (4): 516–26. doi:10.1016/j.humpath.2008.07.018. PMID 19121848. http://linkinghub.elsevier.com/retrieve/pii/S0046-8177(08)00447-4. 
  8. ^ Nakanuma Y, Sasaki M, Terada T, Harada K (1994). "Intrahepatic peribiliary glands of humans. II. Pathological spectrum". J. Gastroenterol. Hepatol. 9 (1): 80–6. PMID 8155873. 
  9. ^ Wanless IR (September 1995). "Terminology of nodular hepatocellular lesions". Hepatology 22 (3): 983–993. doi:10.1002/hep.1840220341. http://onlinelibrary.wiley.com/doi/10.1002/hep.1840220341/abstract. 
  10. ^ a b c d Gastroenterology IWPotWCo (August 1994). "Terminology of chronic hepatitis, hepatic allograft rejection, and nodular lesions of the liver: summary of recommendations developed by an international working party, supported by the World Congresses of Gastroenterology, Los Angeles, 1994". Am. J. Gastroenterol. 89 (8 Suppl): S177–81. PMID 8048409. 
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Translations:

Hepatitis

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Dansk (Danish)
n. - leverbetændelse, hepatitis

Nederlands (Dutch)
hepatitis, ontsteking van de lever

Français (French)
n. - hépatite

Deutsch (German)
n. - Hepatitis, Leberentzündung

Ελληνική (Greek)
n. - (παθολ.) ηπατίτιδα

Italiano (Italian)
epatite

Português (Portuguese)
n. - hepatite (f) (Med.)

Русский (Russian)
гепатит

Español (Spanish)
n. - hepatitis

Svenska (Swedish)
n. - hepatit (inflammation i levern)

中文（简体）(Chinese (Simplified))
肝炎

中文（繁體）(Chinese (Traditional))
n. - 肝炎

한국어 (Korean)
n. - 간염

日本語 (Japanese)
n. - 肝炎

العربيه (Arabic)
‏(الاسم) مرض التهاب الكبد‏

עברית (Hebrew)
n. - ‮דלקת הכבד, צהבת‬

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